FOXP1­induced DUSP12 alleviates vascular endothelial cell inflammation and oxidative stress injury induced by ox­LDL via MAP3K5 signaling pathway.

Atherosclerosis (AS) is a type of chronic inflammatory disease and the main pathological basis of cardiovascular and cerebrovascular diseases, which seriously threaten the health of patients. The dual specificity phosphatase 12 (DUSP12) protein is known as regulator of inflammatory diseases. Nonetheless, at present, there are only a few reports on the regulatory role of DUSP12 in AS. Human umbilical vein endothelial cells (HUVECs) were induced using oxidized low-density lipoprotein (ox-LDL). Subsequently, cell transfection experiments were performed to overexpress DUSP12 in ox-LDL-induced HUVECs. Cell Counting Kit-8, TUNEL western blotting, 2',7'-dichlorofluorescein diacetate assays, ELISA and other techniques were used to measure cell viability, apoptosis, inflammation, oxidative stress and endothelial function-related indicators. Subsequently, the relationship between DUSP12 and Forkhead box P1 (FOXP1) was predicted using the JASPAR database and verified using luciferase reporter and chromatin immunoprecipitation assays. Finally, the regulatory mechanism was investigated by simultaneously overexpressing DUSP12 and knocking down FOXP1 in ox-LDL-induced HUVECs and MAP3K5-related proteins of the DUSP12 downstream pathway were measured by western blotting. The expression of DUSP12 in ox-LDL-induced HUVECs was significantly decreased. Overexpression of DUSP12 inhibited apoptosis, inflammation and oxidative stress damage and alleviated endothelial dysfunction in ox-LDL-induced HUVECs. FOXP1 promoted the transcription of DUSP12. Moreover, FOXP1 alleviated ox-LDL-induced apoptosis, inflammation and oxidative stress damage in HUVECs by regulating the expression of DUSP12, probably acting through the MAP3K5 pathway. Collectively, the present study revealed that FOXP1-induced DUSP12 alleviated vascular endothelial cell inflammation and oxidative stress injury in ox-LDL-induced HUVECs via the MAP3K5 signaling pathway, which might shed novel insights into the targeted treatment for AS in the clinic.

F-box and WD repeat-containing protein 7 ameliorates angiotensin II-induced myocardial hypertrophic injury via the mTOR-mediated autophagy pathway.

Myocardial hypertrophy is a common heart disease that is closely associated with heart failure. The expression of F-box and WD repeat-containing protein 7 (FBW7) is significantly downregulated in angiotensin (Ang) II-induced cardiac fibroblasts, suggesting that it may possess an important function in cardiac development. The present study attempted to explore the role of FBW7 in Ang II-induced myocardial hypertrophic injury and its associated mechanism of action. Reverse transcription-quantitative PCR and western blotting were used to determine the expression levels of FBW7 in Ang II-induced H9C2 cells. The expression levels of autophagy-related and mTOR signaling pathway-related proteins were detected using western blotting. Cell viability was assessed using the Cell Counting Kit-8 assay. The apoptosis rate of H9C2 cells was detected using TUNEL assay and western blotting. Cellular hypertrophy and fibrosis were assessed using phalloidin staining and western blotting. Levels of inflammatory factors were examined using ELISA and western blotting, whereas levels of oxidative stress-related markers were detected by corresponding kits. The results indicated that FBW7 expression was downregulated in Ang II-induced H9C2 cells. FBW7 upregulation enhanced the expression levels of autophagy-related proteins and activated mTOR-mediated cellular autophagy. FBW7 overexpression promoted the cell viability, inhibited Ang II-induced apoptosis, cellular hypertrophy and fibrosis in H9C2 cells via the autophagic pathway, as well as inflammation and oxidative stress. Overall, the data indicated that FBW7 overexpression ameliorated Ang II-induced hypertrophic myocardial injury via the mTOR-mediated autophagic pathway.

S100A1 as a potential biomarker for the diagnosis of patients with acute aortic dissection.

OBJECTIVE: Acute aortic dissection (AAD) is a common life-threatening cardiovascular disease. This retrospective study was conducted to analyze the plasma concentration of S100A1 and its diagnostic value for AAD through receiver operating characteristic (ROC) curve and logistic regression analyses. METHODS: Seventy-eight patients with AAD and 77 healthy controls were included, and the relevant clinical data for each group were collected. According to the Stanford classification, the AAD patients were divided into types A and B. The plasma levels of S100A1, D-dimer, hypersensitive C-reactive protein, and cardiac troponin T were detected by enzyme-linked immunosorbent assays. RESULTS: The S100A1 concentrations in the healthy control, Stanford A, and Stanford B groups were 0.7 ± 0.6, 4.9 ± 2.6, and 3.5 ± 2.2 ng/mL, respectively. The concentration of S100A1 was increased in patients with AAD complicated with aortic regurgitation, pericardial effusion, or in-hospital death. ROC curve analysis showed that the area under the curve was 0.89. Logistic regression analysis revealed that the S100A1 level was an important risk factor for the development of AAD. CONCLUSION: Plasma S100A1 is significantly elevated in patients with AAD, and its concentration has potential clinical value for diagnosing AAD.

Association between serum S100A1 level and Global Registry of Acute Coronary Events score in patients with non-ST-segment elevation acute coronary syndrome.

Objective Acute coronary syndrome (ACS) is associated with several clinical syndromes, one of which is acute non-ST-segment ACS (NSTE-ACS). S100A1 is a calcium-dependent regulator of heart contraction and relaxation. We investigated the association between the serum S100A1 level and the Global Registry of Acute Coronary Events (GRACE) risk score in patients with NSTE-ACS and the potential of using the serum S100A1 level to predict the 30-day prognosis of NSTE-ACS. Methods The clinical characteristics of 162 patients with NSTE-ACS were analyzed to determine the GRACE score. The serum S100A1 concentration was determined using fasting antecubital venous blood. The patients were divided into different groups according to the serum S100A1 level, and the 30-day NSTE-ACS prognosis was evaluated using Kaplan-Meier analysis. Results The serum S100A1 levels differed significantly among the groups. Correlation analysis showed that the serum S100A1 level was positively correlated with the GRACE score. Kaplan-Meier analysis revealed that the number of 30-day cardiac events was significantly higher in patients with an S100A1 level of >3.41 ng/mL. Conclusions S100A1 is a potential biomarker that can predict the progression of NSTE-ACS and aid in its early risk stratification and prognosis.

Total Endovascular Repair of Post-dissection Aortic Arch Aneurysm With Chimney Technique.

Open surgery remains the standard procedure for treatment of aortic arch pathologies. However, total endovascular repair can be a safe option for patients who are poor candidates for surgery because of compromised physiology. We report the case of a 63-year-old man with a post-dissection aortic arch aneurysm. We repaired the aneurysm using thoracic endovascular aortic repair (TEVAR) and used the chimney technique to reconstruct the supra-aortic branches. The patient is doing well after 12-month follow-up, demonstrating that TEVAR with the chimney technique can be used successfully for the treatment of post-dissection arch aneurysm.